Release of atrial natriuretic factor is primarily regulated by mechanical changes in atrial wall tension during the atrial cycle, with humoral factors playing a secondary role.
The cardiac atria synthesize and store a hormone termed atrial natriuretic factor (ANF). ANF is released into the systemic circulation, and the circulating 28 amino acid peptide can be measured by radioimmunoassay. The hormone participates in body fluid homeostasis through its effect on renal sodium excretion and by inducing a shift of circulating fluid to the interstitial space. Release of ANF is mainly regulated by mechanical changes in the left and right atrial wall. It has been demonstrated that ANF release is related to changes in atrial wall tension occurring during each atrial cycle, and therefore, release of ANF will increase with increasing heart rate. Not only the increase in wall tension during passive atrial distension (v wave), but also the increase in tension during atrial systole (a wave) are determinants of ANF release. The mechanochemical transducer is most likely located in the atrial myocytes, but its nature is unknown. There is no evidence to suggest that efferent cardiac nerves are essential in the regulation of ANF release. Humoral factors have been suggested as regulators of ANF release, particularly catecholamines and angiotensin II. A receptor-mediated direct stimulatory effect of alpha-adrenergic stimulation and an inhibitory effect of beta-adrenergic stimulation have been demonstrated, but these direct effects are small compared to the effect of changes in atrial wall tension. Circulating catecholamines and angiotensin II stimulate ANF release mainly through their haemodynamic effects.
Geir Christensen (Fri,) reported a review. Atrial natriuretic factor was evaluated. Release of atrial natriuretic factor is primarily regulated by mechanical changes in atrial wall tension during the atrial cycle, with humoral factors playing a secondary role.